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Identification of temperature compensation mechanisms in the mammalian circadian clock

Research Project

Project/Area Number 15K08212
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Environmental physiology(including physical medicine and nutritional physiology)
Research InstitutionKyoto Prefectural University of Medicine

Principal Investigator

Tsuchiya Yoshiki  京都府立医科大学, 医学(系)研究科(研究院), 講師 (30456777)

Co-Investigator(Renkei-kenkyūsha) YAGITA Kazuhiro  京都府立医科大学, 大学院医学研究科, 教授 (90324920)
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords概日リズム / 温度補償性
Outline of Final Research Achievements

In this study, we aimed to reveal mechanisms underlying temperature compensation of the mammalian circadian clock. We established a series of mouse embryonic stem cell (ESC) lines with single or multiplex clock gene ablations. ESC-based in vitro circadian clock formation assay reveals that complexed mutations, such as the CKIδ:CKIε:Cry2 mutant, exhibit an additively lengthened circadian period. By using these mutant cells, we also investigated the relation between period-length alteration and temperature compensation. Although CKIδ deficient cells slightly affected the temperature-insensitivity of period-length, we demonstrated that the temperature compensation property is largely maintained in all mutants. These results show that the ESC-based assay system could offer a more systematic and comprehensive approach to the genotype-chronotype analysis of the intracellular circadian clockwork in mammals.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (3 results)

All 2016 2015

All Journal Article (2 results) (of which Peer Reviewed: 2 results,  Acknowledgement Compliant: 2 results,  Open Access: 1 results) Presentation (1 results)

  • [Journal Article] Effect of Multiple clock gene ablations on the circadian period-length and temperature compensation in mammalian cells.2016

    • Author(s)
      Tsuchiya Y., Umemura Y., Minami Y., Koike N., Hosokawa T., Hara M., Ito H., Inokawa H. & Yagita K.
    • Journal Title

      Journal of Biological Rhythms

      Volume: 31 Issue: 1 Pages: 48-56

    • DOI

      10.1177/0748730415613888

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Acknowledgement Compliant
  • [Journal Article] Disruption of MeCP2 attenuates circadian rhythm in CRISPR/Cas9-based Rett syndrome model mouse.2015

    • Author(s)
      Tsuchiya Y., Minami Y., Umemura Y., Watanabe H., Ono D., Nakamura W., Takahashi T., Honma S., Kondoh G., Matsuishi T. & Yagita K.
    • Journal Title

      Genes to Cells

      Volume: 20 Issue: 12 Pages: 992-1005

    • DOI

      10.1111/gtc.12305

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Presentation] The CRISPR/Cas9-mediated disruption of clock genes in mouse ES cells.2015

    • Author(s)
      土谷佳樹
    • Organizer
      第22回日本時間生物学会学術大会
    • Place of Presentation
      東京
    • Year and Date
      2015-11-21
    • Related Report
      2015 Research-status Report

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Published: 2015-04-16   Modified: 2019-03-29  

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